General principles of asynchronous activation and preexcitation

Jan 8, 1998

Conduction defects are generally due to asynchronous activation of the ventricles. This problem can be induced by one of two mechanisms: delayed activation of an area of the ventricles or early activation (preexcitation) of an area of the ventricles.

ASYNCHRONOUS ACTIVATION DUE TO DELAYED ACTIVATION — Delayed activation producing asynchronous activation may be a result of anatomic abnormalities or of physiologic properties of the cardiac tissues. After an impulse emerges from the atrioventricular (AV) node, it traverses the His bundle, and propagates down the bundle branches and the fascicles of the bundle branches to the terminal Purkinje fibers and ultimately the ventricular myocardium. Delayed or blocked conduction in the bundles or their fascicles results in asynchronous activation and repolarization of the right and left ventricles.  This, in turn, gives rise to characteristic electrocardiographic patterns. Examples of delayed activation include:

  •  Right or left bundle branch block
  •  Fascicular block
  •  Peri-infarction block (occurring in the area of a myocardial infarction)
  •  Parietal block (reflecting disease in the terminal Purkinje system).

Two factors – magnitude and duration – determine the electrocardiographic (ECG) and vectorcardiographic (VCG) changes seen with a given type of block.

Magnitude — The magnitude (or amplitude) of the extracellular signal generated by the wavefront of unopposed dipoles can be affected by a number of factors. Examples include:

  •  A gain of force as with ventricular enlargement.
  •  A loss of force as with myocardial infarction.
  •  A change in cancellation due to asynchrony that can increase or decrease unopposed dipoles.

With regard to cancellation, the term "activation" is used to describe those unopposed boundaries that result in an electrocardiographically recorded potential. Many other wavefronts exist, however, and "cancel" each other. Normal synchronous ventricular depolarization results in a predictable sequence of opposed and unopposed wavefronts that result in the normal ECG and VCG [1,2]. Asynchronous activation generally reduces the amount of signal cancellation, resulting in a larger extracellularly recorded electrogram. With left bundle block, for example, left ventricular activation is delayed, occurring later than activation of the right bundle. As a result, the left ventricular signal is not partially canceled by that from the right ventricle, leading to an increase in amplitude of the QRS complex. This is the reason that standard voltage criteria for ventricular enlargement are invalid in bundle branch blocks.

Duration — Asynchronous activation can also affect the duration of the recorded potential. The time of initiation of activation is unchanged in this setting, but termination is delayed due to slower conduction to the blocked ventricle. The net effect is increased duration of the P wave or QRS complex, depending upon the site of disease.

ASYNCHRONOUS ACTIVATION DUE TO PREEXCITATION — The normal temporal and spatial sequence of atrial and ventricular activation can be altered by anomalous conduction between the atria and ventricles. The preexcitation syndromes are conditions in which atrial activation of the ventricles occurs earlier than would be expected if atrioventricular conduction occurred normally through the atrioventricular (AV) node. Preexcitation of the ventricles commonly occurs because the impulse travels from the atria to the ventricles through accessory pathways. It has been suggested that preexcitation can also be produced by longitudinal dissociation of the AV node and dual AV nodal pathways.

General anatomic considerations — A number of conducting pathways have been described. These include:

  •  Accessory atrioventricular connections, often called Kent bundles in the older literature, which directly connect the atria and ventricles [3,4,5].

  •  James fibers, which connect the atria with the low AV node (atrionodal accessory pathway) or the bundle of His (atriofascicular accessory pathway) [6].

  •  So-called Mahaim fibers of several types that arise either from the AV node and insert into ventricular tissue (nodoventricular accessory pathways) or from one of the bundle branches and insert into ventricular tissue (fasciculoventricular accessory pathway) [7,8,9].

Terminology based upon anatomic connections is gradually replacing the venerable eponyms and some attempt has been made at standardization [7]. The European Study Group for Preexcitation suggests that the term "connection" should be used to describe pathways that insert into ventricular myocardium while "tracts" should be applied to pathways that insert into specialized conduction tissue [10]; however, the terms are often used interchangeably and tract is increasingly replacing connection (show figure 1) [11].

The concepts, however, have undergone some change. The atrioventricular accessory pathways are involved in preexcitation and in reentrant rhythms. The clinical tachycardias and preexcitation ascribed to the James and Mahaim fibers are uncertain.

Atrioventricular accessory pathways — Ninety-five percent of atrioventricular accessory pathways conduct rapidly and have the characteristics of INa (sodium) dependent phase 0 action potentials that occur in normal "fast response" myocardium. (See "Myocardial action potential and action of antiarrhythmic drugs"). Five percent show decremental conduction, the mechanism of which is uncertain. Possible explanations include geometric factors, partial inactivation of the sodium channel, or perhaps dependence on a calcium channel. The fast response pathways often have short refractory periods and can conduct rapidly. This poses a particular problem in rapid supraventricular tachycardias such as atrial flutter, which may conduct 1:1, and atrial fibrillation, which may produce ventricular flutter and fibrillation.

In preexcitation syndromes in which the accessory pathway inserts eccentrically, the resultant ventricular depolarization represents a fusion between ventricular activation initiated by the fast response, rapidly conducting bypass pathway and that initiated by the slow response, slowly conducting atrioventricular node. This is the pattern characteristic of patients with the Wolff-Parkinson-White syndrome. The principles of this fusion are illustrated in Figure 2 (show figure 2A-2C).

  •  The PR interval is shortened due to the preexcitation.
  •  The eccentric ventricular activation results in a slurred upstroke of the QRS or delta wave.
  •  The QRS duration is increased due to the asynchronous activation between the preexcited and normally excited portions of the ventricular myocardium.

How the electrocardiogram can be used to identify the location of the accessory pathway is discussed elsewhere. (See "Pathophysiology and mapping of accessory pathways in the preexcitation syndrome")

James fibers and the Lown-Ganong-Levine syndrome — The Lown-Ganong-Levine syndrome is characterized by palpitations in patients with an ECG that shows a short PR interval and a normal QRS duration [12]. For many years, this disorder was thought to be due to tracts that connected the atrium with the low AV node or the His bundle (via James fibers) [6].

The current concept, however, is that the short PR interval with a normal QRS pattern results, in most cases, from enhanced or accelerated AV nodal conduction and less often from an accessory pathway [11,13,14,15]. A short PR interval appears to be more frequent in patients with concealed accessory pathways [14], but has also been associated with dual pathway physiology and AV nodal reentrant tachycardia. However, only patients with symptomatic tachyarrhythmias are studied electrophysiologically; as a result, it is uncertain whether all individuals with a short PR interval and normal QRS complex have enhanced AV nodal conduction or accessory pathways near the AV node.

Role of Mahaim fibers — The issue of the Mahaim pathways, which arise from the AV node or one of the bundle branches and insert into ventricular tissue, has been reviewed in detail [9]. It was presumed that these pathways could explain patients in whom the PR interval was normal (because the AV node was normally traversed) but the QRS was widened (presumably due to eccentric activation of the ventricles) [16]. Some patients also had a prolonged PR interval with eccentric ventricular activation. This could be explained by slowed AV nodal conduction and anomalous connections at the level of or below the AV node.

However, surgical [17,18] and more recent catheter ablation studies [19,20,21,22] suggest that electrophysiologic characteristics attributed to nodoventricular Mahaim fibers are due to atriofascicular accessory connections with decremental conduction. One report, for example, suggests the presence of an atrioventricular connection in the tricuspid ring [19].  This connection has slow and rate-dependent conduction, blocks with adenosine, has intrinsic automaticity, and links to a rapidly conducting insulated pathway that generates a "His-like" potential. Despite these observations, some experts still believe that nodofascicular tracts exist and are functional [11].

Classification of arrhythmias associated with accessory pathways — The accessory pathways have two effects which facilitate the development of certain supraventricular tachyarrhythmias: they can provide a pathway for reentry; and they can produce preexcitation, which results in a wide complex tachycardia.

The atrioventricular reentrant tachycardias (AVRT) can utilize both the AV node and an accessory pathway in the reentrant circuit. (See "Tachyarrhythmias associated with the Wolff-Parkinson-White syndrome").

  •  Orthodromic AVRT, the most common form, uses a circuit consisting of antegrade conduction through the AV node and retrograde conduction through the accessory pathway. In the absence of preexisting or functional bundle branch block, this produces a narrow QRS tachycardia in which the P wave follows the QRS complex (show figure 3).

  •  The less common or antidromic form of AVRT conducts antegrade through the accessory pathway and retrograde through the AV node, producing a wide QRS complex with a delta wave and a P wave that follows the QRS complex. This would be a reentrant form of a "preexcited tachycardia" that uses the AV node (see below) (show figure 4).

  •  The permanent form of junctional reciprocating tachycardia is a variant of AVRT. It uses anomalous connections as evidenced by successful interruption of the arrhythmia after ablation of the responsible accessory pathways [23].

Preexcited tachycardias — Preexcited tachycardias, such as the WPW syndrome, are wide complex tachycardias that conduct antegrade over the accessory pathway. They are induced by supraventricular tachycardias, including atrial fibrillation, atrial flutter, and the family of atrial tachycardias including the antidromic form of AVRT. (See "Pathophysiology and mapping of accessory pathways in the preexcitation syndrome" and see "Tachyarrhythmias associated with the Wolff-Parkinson-White syndrome").